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甜菊糖苷通过调节金黄色葡萄球菌感染的小鼠乳腺上皮细胞中的TLR2及TLR2相关蛋白来抑制炎症和细胞凋亡。

Stevioside inhibits inflammation and apoptosis by regulating TLR2 and TLR2-related proteins in S. aureus-infected mouse mammary epithelial cells.

作者信息

Wang Tiancheng, Song Xiaojing, Zhang Zecai, Guo Mengyao, Jiang Haichao, Wang Wei, Cao Yongguo, Zhu Lianqin, Zhang Naisheng

机构信息

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin Province 130062, People's Republic of China.

College of Animal Science and Technology, Qingdao Agriculture University, Qingdao, Shandong Province 266109, People's Republic of China.

出版信息

Int Immunopharmacol. 2014 Sep;22(1):192-9. doi: 10.1016/j.intimp.2014.06.015. Epub 2014 Jun 27.

Abstract

Stevioside is a natural sweetener that is commonly used in traditional medicine and as a food additive. The object of this study was to investigate the anti-inflammatory and anti-apoptosis function of stevioside and the possible molecular mechanisms for such activity in Staphylococcus aureus (S. aureus)-infected mouse mammary epithelial cells (MMECs). The cells were treated with varying doses of stevioside before infection with S. aureus. The live/dead cells were detected by immunofluorescence microscopy. The pro-inflammatory cytokines were determined by ELISA. The mRNA of TLR2 and proteins related to NF-κB, MAPK and apoptosis were analyzed by q-PCR. The relative protein expression levels were determined by Western blot. The results indicated that stevioside inhibited the mRNA and protein expression of TNF-α, IL-6 and IL-1β dose-dependently in S. aureus-stimulated MMECs. Stevioside suppressed the S. aureus-induced expression of TLR2 and proteins of the NF-κB and MAPK pathways as well as apoptosis. The mRNA levels of IκBα, p38, ERK, JNK, p65, caspase-3 and Bax were not influenced by the stevioside treatment. Stevioside exerts anti-inflammatory and anti-apoptotic properties by inhibiting the release of cytokines and the activation of TLR2 and proteins of the NF-κB and MAPK signaling pathways, as well as caspase-3 and Bax.

摘要

甜菊糖苷是一种天然甜味剂,常用于传统医学和作为食品添加剂。本研究的目的是探讨甜菊糖苷在金黄色葡萄球菌感染的小鼠乳腺上皮细胞(MMECs)中的抗炎和抗凋亡功能以及这种活性的可能分子机制。在感染金黄色葡萄球菌之前,用不同剂量的甜菊糖苷处理细胞。通过免疫荧光显微镜检测活/死细胞。通过ELISA测定促炎细胞因子。通过q-PCR分析TLR2的mRNA以及与NF-κB、MAPK和凋亡相关的蛋白质。通过蛋白质印迹法测定相对蛋白质表达水平。结果表明,甜菊糖苷在金黄色葡萄球菌刺激的MMECs中剂量依赖性地抑制TNF-α、IL-6和IL-1β的mRNA和蛋白质表达。甜菊糖苷抑制金黄色葡萄球菌诱导的TLR2表达以及NF-κB和MAPK途径的蛋白质表达以及凋亡。IκBα、p38、ERK、JNK、p65、caspase-3和Bax的mRNA水平不受甜菊糖苷处理的影响。甜菊糖苷通过抑制细胞因子的释放以及TLR2和NF-κB和MAPK信号通路的蛋白质以及caspase-3和Bax的激活发挥抗炎和抗凋亡特性。

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